Oncogenic activation of the STAT3 pathway drives PD-L1 expression in natural killer/T-cell lymphoma
Tammy Song, Maarja-Liisa Nairismägi, Yurike Laurensia, Jing Quan Lim, Jing Tan(Sun Yat-sen University), Zhi-Mei Li(National Cancer Centre Singapore), Wan‐Lu Pang, Atish Kizhakeyil(Nanyang Technological University), Giovani-Claresta Wijaya(National Cancer Centre Singapore), Da-Chuan Huang(National Cancer Centre Singapore), Sanjanaa Nagarajan(National Cancer Centre Singapore), Burton Kuan Hui Chia, Daryl Ming Zhe Cheah, Yan Hui Liu(Guangdong General Hospital), Fen Zhang(Guangdong General Hospital), Hui-Lan Rao(Sun Yat-sen University), Tiffany Tang(National Cancer Centre Singapore), Esther Kam-Yin Wong, Jin‐Xin Bei(Sun Yat-sen University), Jabed Iqbal(Singapore General Hospital), Nicholas-Francis Grigoropoulos(Singapore General Hospital), Siok‐Bian Ng(Yong In University), Wee Joo Chng(National University of Singapore), Bin Tean Teh(Duke-NUS Medical School), Soo‐Yong Tan(Yong In University), Navin Kumar Verma(Nanyang Technological University), Hao Fan(Agency for Science, Technology and Research), Soon Thye Lim(Duke-NUS Medical School), Choon Kiat Ong(Agency for Science, Technology and Research)
Cited by 319Open Access
Abstract
mutant NKTL cell lines. In NKTL tumors, STAT3 activation correlated significantly with PD-L1 expression. We demonstrated that STAT3 activation confers high PD-L1 expression, which may promote tumor immune evasion. The combination of PD-1/PD-L1 antibodies and STAT3 inhibitors might be a promising therapeutic approach for NKTL, and possibly PTCL.
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